- •Foreword
- •Preface
- •List of Contributors
- •Acknowledgments
- •Dedication
- •In Memorium
- •DEFINITIONS
- •EPIDEMIOLOGIC AND SOCIOECONOMIC ASPECTS OF THE GLAUCOMAS
- •RISK FACTORS
- •CLASSIFICATION OF THE GLAUCOMAS
- •REFERENCES
- •Aqueous humor formation
- •FUNCTION OF AQUEOUS HUMOR
- •ANATOMY OF THE CILIARY BODY
- •STRUCTURE
- •ULTRASTRUCTURE OF THE CILIARY PROCESSES
- •VASCULAR SUPPLY
- •MECHANISM OF AQUEOUS FORMATION
- •ULTRAFILTRATION
- •ACTIVE TRANSPORT
- •DIFFUSION
- •CHEMICAL COMPOSITION OF THE AQUEOUS HUMOR
- •THE BLOOD–AQUEOUS BARRIER
- •PRESSURE-DEPENDENT TECHNIQUES
- •Tonography
- •Suction cup
- •Perfusion
- •TRACER METHODS
- •Photogrammetry
- •Radiolabeled isotopes
- •Fluorescein
- •Fluoresceinated dextrans
- •Paraminohippurate
- •Iodide
- •FACTORS AFFECTING AQUEOUS HUMOR FORMATION
- •DIURNAL VARIATION
- •INTRAOCULAR PRESSURE/PSEUDOFACILITY
- •BLOOD FLOW TO THE CILIARY BODY
- •NEURAL CONTROL
- •HORMONAL EFFECTS
- •INTRACELLULAR REGULATORS
- •CLINICAL ASPECTS OF AQUEOUS HUMOR FORMATION
- •CLINICAL CONDITIONS
- •PHARMACOLOGIC AGENTS
- •SURGERY
- •REFERENCES
- •PHYSIOLOGY ISSUES UNIQUE TO THE CONVENTIONAL AQUEOUS OUTFLOW SYSTEM
- •FUNCTIONS OF THE CONVENTIONAL AQUEOUS OUTFLOW SYSTEM
- •ANATOMY OF THE CONVENTIONAL OUTFLOW SYSTEM
- •SCHWALBE’S LINE
- •SCLERAL SPUR
- •TRABECULAR MESHWORK TISSUES
- •Uveal meshwork
- •Corneoscleral meshwork
- •Uveal and corneoscleral meshwork ultrastructure
- •Juxtacanalicular space and cells
- •SCHLEMM’S CANAL
- •Overview
- •Schlemm’s canal inner wall endothelium
- •Glycocalyx
- •Distending cells that form invaginations or pseudovacuoles, ‘giant vacuoles’
- •Schlemm’s canal endothelium pores
- •Sonderman’s canals invaginate into the trabecular meshwork
- •Septa
- •Schlemm’s canal valves spanning across Schlemm’s canal
- •Herniations or protrusions of Schlemm’s canal inner wall
- •Collector channels, aqueous veins and episcleral veins
- •RESISTANCE SITES IN THE AQUEOUS OUTFLOW SYSTEM
- •JUXTACANALICULAR SPACE RESISTANCE
- •SCHLEMM’S CANAL ENDOTHELIUM RESISTANCE
- •PRINCIPLES OF BIOMECHANICS AS A METHODOLOGY TO IDENTIFY TISSUE RESISTANCE
- •TISSUE LOADING STUDIES
- •BOUNDARY CONDITIONS
- •EVIDENCE FROM EXPERIMENTAL MICROSURGERY
- •AQUEOUS OUTFLOW PHYSIOLOGY: PASSIVE AND DYNAMIC FLOW MODELS
- •THE AQUEOUS OUTFLOW SYSTEM AS A PASSIVE FILTER
- •THE AQUEOUS OUTFLOW SYSTEM AS A DYNAMIC MECHANICAL PUMP
- •EXTRINSIC PRESSURE REGULATION MECHANISMS
- •UVEOSCLERAL FLOW
- •METHODS FOR MEASURING FACILITY OF OUTFLOW
- •FACILITY OF OUTFLOW CALCULATIONS
- •Tonography
- •Perfusion
- •Suction cup
- •FACILITY OF OUTFLOW AND ITS CLINICAL IMPLICATIONS
- •FACTORS AFFECTING THE FACILITY OF OUTFLOW
- •HORMONES
- •CILIARY MUSCLE TONE
- •DRUGS
- •SURGICAL THERAPY
- •DIURNAL FLUCTUATION
- •GLAUCOMA
- •EPISCLERAL VENOUS PRESSURE
- •REFERENCES
- •Intraocular pressure
- •INSTRUMENTS FOR MEASURING INTRAOCULAR PRESSURE
- •APPLANATION INSTRUMENTS
- •Goldmann tonometer
- •Perkins tonometer
- •Draeger tonometer
- •MacKay-Marg and Tono-Pen™ tonometers
- •Pneumatic tonometer
- •Non-contact tonometer
- •The Ocuton™ tonometer
- •Maklakow tonometer
- •INDENTATION INSTRUMENTS
- •Schiøtz tonometer
- •Electronic Schiøtz tonometer
- •Impact–rebound tonometer
- •Transpalpebral tonometry
- •DYNAMIC CONTOUR TONOMETRY
- •CONTINUOUS MONITORING OF INTRAOCULAR PRESSURE
- •SUMMARY OF TONOMETRY
- •DISTRIBUTION OF INTRAOCULAR PRESSURE IN THE GENERAL POPULATION
- •FACTORS THAT INFLUENCE INTRAOCULAR PRESSURE
- •RACE
- •HEREDITY
- •DIURNAL VARIATION
- •SEASONAL VARIATION
- •CARDIOVASCULAR FACTORS
- •EXERCISE
- •WIND INSTRUMENT PLAYING
- •LIFESTYLE
- •POSTURAL CHANGES
- •NEURAL FACTORS
- •PSYCHIATRIC DISORDERS
- •HORMONAL FACTORS
- •REFRACTIVE ERROR
- •FOODS AND DRUGS
- •MISCELLANEOUS
- •EYE MOVEMENTS
- •EYELID CLOSURE
- •INFLAMMATION
- •SURGERY
- •REFERENCES
- •Gonioscopic anatomy
- •GROSS ANATOMY
- •ANATOMIC FEATURES OF NORMAL EYES
- •GONIOSCOPIC ANATOMY AND MICROSCOPIC INTERPRETATION
- •PUPIL AND IRIS
- •CILIARY BODY, IRIS PROCESSES, AND SYNECHIAE
- •SCLERAL SPUR
- •SCHWALBE’S LINE
- •TRABECULAR MESHWORK AND TRABECULAR PIGMENT BAND
- •GONIOSCOPIC APPEARANCE
- •REFERENCES
- •Methods of gonioscopy
- •DEFINITION
- •METHODS OF GONIOSCOPY
- •EQUIPMENT
- •Goldmann and Zeiss lenses (indirect method)
- •Koeppe lens (direct method)
- •TECHNIQUE
- •Indirect gonioscopic lenses
- •Indentation (compression) gonioscopy
- •Direct gonioscopic lens
- •REFERENCES
- •GRADING OF CHAMBER ANGLE
- •DIAGRAMMING ANGLE WIDTH, SYNECHIAE, AND PIGMENTATION
- •TRABECULAR PIGMENT BAND
- •SPAETH CLASSIFICATION
- •STEP 4: TRABECULAR MESHWORK PIGMENTATION
- •EXAMPLES
- •DIFFICULTIES AND ARTIFACTS IN GONIOSCOPY
- •CLINICAL USEFULNESS OF GONIOSCOPY
- •AID IN DIAGNOSIS OF TYPE OF GLAUCOMA
- •EVALUATION OF SYMPTOMS
- •USE OF DRUGS
- •POSTOPERATIVE EXAMINATIONS
- •CONDITIONS OTHER THAN GLAUCOMA
- •SUMMARY OF IMPORTANT GONIOSCOPIC TECHNIQUES
- •REFERENCES
- •APPENDIX
- •Visual field theory and methods
- •THE NORMAL VISUAL FIELD
- •VISUAL ACUITY VERSUS VISUAL FIELD
- •TERMINOLOGY AND DEFINITIONS
- •THEORY OF VISUAL FIELD TESTING
- •KINETIC PERIMETRY
- •STATIC PERIMETRY
- •THRESHOLD-RELATED TESTING
- •ZONE TESTING
- •SCREENING TESTS
- •OTHER STATIC TESTING TECHNIQUES
- •THE FUTURE OF VISUAL FIELD TESTING
- •COMBINED STATIC AND KINETIC PERIMETRY
- •REFERENCES
- •PATIENT VARIABLES
- •FIXATION
- •RELIABILITY
- •OCULAR VARIABLES
- •PUPIL SIZE
- •MEDIA CLARITY
- •REFRACTIVE CORRECTION
- •TESTING VARIABLES
- •TECHNICIAN
- •BACKGROUND ILLUMINATION
- •STIMULUS SIZE AND INTENSITY
- •STIMULUS EXPOSURE TIME
- •AREA TESTED
- •EQUIPMENT AND TECHNIQUES
- •GENERAL PRINCIPLES
- •TANGENT SCREEN
- •BOWL PERIMETRY
- •Preparing the patient
- •Technique of computerized bowl perimetry
- •REFERENCES
- •Visual field interpretation
- •GLAUCOMATOUS CHANGES IN THE VISUAL FIELD
- •ANATOMY OF VISUAL FIELD DEFECTS
- •TYPES OF VISUAL FIELD LOSS
- •Generalized loss
- •Localized defects (scotomata)
- •GLAUCOMATOUS VISUAL FIELD DEFECTS
- •Generalized depression
- •Irregularity of the visual field
- •Nasal step or depression
- •Temporal step or depression
- •Enlargement of the blind spot
- •Isolated paracentral scotomata
- •Arcuate defects (nerve fiber bundle defects)
- •End-stage defects
- •Central and temporal islands
- •Reversal of visual field defects
- •ANALYSIS OF VISUAL FIELD LOSS
- •CHRONIC OPEN-ANGLE GLAUCOMA
- •ANGLE-CLOSURE GLAUCOMA
- •OTHER CAUSES
- •ESTERMAN DISABILITY RATING
- •ANALYSIS OF COMPUTERIZED STATIC PERIMETRY
- •RELIABILITY INDEXES
- •False-positive and false-negative responses
- •Fixation reliability
- •FLUCTUATION
- •Short-term fluctuation
- •Long-term fluctuation
- •GLOBAL INDEXES
- •Mean sensitivity
- •Mean deviation or defect
- •Standard deviation or variance
- •GRAPHIC PLOTS
- •AREA OF THE VISUAL FIELD TO BE TESTED
- •LONG-TERM ANALYSIS
- •DETERMINATION OF NORMAL VISUAL FIELD
- •DEVIATION FROM NORMAL VALUES
- •Graphic plot of points varying from normal
- •Global indexes
- •Comparison with the other eye
- •Localized variation within the visual field
- •RECOGNITION OF CHANGE
- •QUANTIFYING VISUAL FIELD CHANGE
- •THE FUTURE OF COMPUTERIZED PERIMETRY
- •REFERENCES
- •Other psychophysical tests
- •INTRODUCTION
- •COLOR VISION AND SHORT-WAVELENGTH AUTOMATED PERIMETRY
- •FREQUENCY-DOUBLING PERIMETRY
- •OTHER PSYCHOPHYSICAL TESTS
- •HIGH-PASS RESOLUTION PERIMETRY
- •MOTION DETECTION PERIMETRY
- •ELECTROPHYSIOLOGY
- •The electroretinogram (ERG)
- •The pattern electroretinogram (PERG)
- •The multifocal electroretinogram (mfERG)
- •The multifocal visual-evoked potential (mfVEP)
- •REFERENCES
- •ANATOMY OF THE OPTIC NERVE HEAD
- •WHERE ARE THE GANGLION CELLS INJURED?
- •WHAT INJURES GANGLION CELLS?
- •Ganglion Cell Susceptibility
- •Connective tissue structures within the optic nerve head
- •Vascular nutrition of the optic disc
- •REFERENCES
- •CLINICAL TECHNIQUES OF EVALUATION
- •OPTIC DISC CHANGES IN GLAUCOMA
- •INTRAPAPILLARY DISC CHANGES
- •Optic disc size
- •Optic disc shape
- •Neuroretinal rim size (NRR)
- •Neuroretinal rim shape
- •Optic cup size in relation to optic disc size
- •Optic cup configuration and depth
- •Cup:disc ratios
- •Position of central retinal vessels and branches
- •PERIPAPILLARY DISC CHANGES
- •Optic disc hemorrhages
- •Nerve fiber layer defects
- •Diameter of retinal arterioles
- •Peripapillary choroidal atrophy
- •PATTERNS OF OPTIC NERVE CHANGES AND SUBTYPES OF GLAUCOMA
- •HIGH MYOPIA DISC PATTERN
- •FOCAL NORMAL-PRESSURE PATTERN (FOCAL ISCHEMIC)
- •AGE-RELATED ATROPHIC PRIMARY OPEN-ANGLE GLAUCOMA PATTERN (SENILE SCLEROTIC)
- •JUVENILE OPEN-ANGLE GLAUCOMA PATTERN
- •PRIMARY OPEN-ANGLE GLAUCOMA PATTERN (GENERALIZED ENLARGEMENT)
- •REFERENCES
- •Optic nerve imaging
- •CONFOCAL SCANNING LASER OPHTHALMOSCOPY (CSLO)
- •HEIDELBERG RETINA TOMOGRAPHY (HRT)
- •Components of the HRT report
- •Evaluating scan quality
- •Strengths and limitations
- •New developments
- •Testing from the patient’s perspective
- •OPTICAL COHERENCE TOMOGRAPHY (OCT)
- •DIFFERENT SCANNING MODALITIES
- •Peripapillary scan
- •Macular scan
- •ONH scan
- •Fast scans
- •COMPONENTS OF THE OCT REPORT
- •RNFL thickness average analysis
- •Macular analysis
- •Optic nerve head analysis
- •QUALITY ASSESSMENT
- •STRENGTHS AND LIMITATIONS
- •TESTING FROM THE PATIENT’S PERSPECTIVE
- •LONGITUDINAL EVALUATIONS
- •SCANNING LASER POLARIMETRY
- •Components of the GDX report
- •Quality assessment
- •Strengths and limitations
- •Testing from the patient’s perspective
- •CONCLUSIONS
- •REFERENCES
- •Primary angle-closure glaucoma
- •HISTORICAL REVIEW AND CLASSIFICATIONS
- •CLASSIFICATIONS OF ANGLE-CLOSURE DISEASE
- •TWENTY-FIRST CENTURY CONSENSUS CLASSIFICATION
- •CLARIFICATIONS AND COMMENTARY
- •PRESENTATIONS OF PRIMARY ANGLE-CLOSURE DISEASE
- •NEW IMAGING TECHNOLOGIES
- •CLASSIFICATION BY MECHANISMS IN THE ANTERIOR SEGMENT
- •PUPILLARY BLOCK GLAUCOMA
- •Epidemiologic studies
- •Demographic risk factors
- •Gender
- •Heredity
- •Refractive error
- •Miscellaneous factors
- •Ocular risk factors and mechanisms
- •Iris bowing and lens–iris channel
- •Provocative tests
- •Clinical presentations of acute PACG with pupillary block
- •Signs and symptoms
- •Clinical examination
- •Treatment of acute PACG
- •Medical management of acute PACG
- •Slit-lamp maneuvers in management of acute PACG
- •Laser interventions for acute PACG
- •Surgical management of PACG
- •Management of the fellow eye
- •Sequelae of acute PACG
- •Correlating older and newer terminologies for angle closure
- •PLATEAU IRIS
- •Plateau iris configuration
- •Plateau iris syndrome
- •Pseudoplateau iris (cysts of the iris and ciliary body)
- •PHACOMORPHIC GLAUCOMA
- •Intumescent and swollen lens
- •REFERENCES
- •OVERVIEW OF TERMS AND MECHANISMS
- •ANTERIOR PULLING MECHANISM
- •NEOVASCULAR GLAUCOMA
- •Histopathology
- •Pathogenesis
- •Conditions and diseases commonly associated with neovascular glaucoma
- •Diabetes mellitus
- •Central retinal vein occlusion
- •Carotid occlusive disease
- •Ocular ischemic syndrome
- •Central retinal artery occlusion
- •Miscellaneous
- •Clinical presentation
- •Treatment
- •IRIDOCORNEAL ENDOTHELIAL SYNDROME
- •Histopathology
- •Pathogenesis
- •Clinical presentation
- •Progressive (essential) iris atrophy
- •Chandler’s syndrome
- •Cogan-Reese syndrome
- •Treatment
- •POSTERIOR POLYMORPHOUS DYSTROPHY
- •Histopathology
- •Pathogenesis
- •Clinical presentation
- •Treatment
- •EPITHELIAL DOWNGROWTH
- •Pathophysiology
- •Histopathology
- •Clinical presentation
- •Treatment
- •FIBROVASCULAR INGROWTH
- •FLAT ANTERIOR CHAMBER
- •INFLAMMATION
- •PENETRATING KERATOPLASTY
- •IRIDOSCHISIS
- •ANIRIDIA
- •POSTERIOR PUSHING (OR ROTATIONAL) MECHANISM
- •CILIARY BLOCK GLAUCOMA (AQUEOUS MISDIRECTION OR MALIGNANT GLAUCOMA)
- •INTRAOCULAR TUMORS
- •NANOPHTHALMOS
- •SUPRACHOROIDAL HEMORRHAGE
- •POSTERIOR SEGMENT INFLAMMATORY DISEASE
- •Treatment
- •CENTRAL RETINAL VEIN OCCLUSION
- •SCLERAL BUCKLING PROCEDURE
- •PANRETINAL PHOTOCOAGULATION
- •RETINOPATHY OF PREMATURITY
- •PUPILLARY BLOCK MECHANISMS
- •Secondary pupillary block glaucoma: iris–lens adhesions
- •Dislocated and subluxed lens
- •Ectopia lentis
- •Microspherophakia
- •REFERENCES
- •Primary open angle glaucoma
- •EPIDEMIOLOGY
- •PREVALENCE
- •PATHOPHYSIOLOGY
- •DIMINISHED AQUEOUS HUMOR OUTFLOW FACILITY
- •Altered corticosteroid metabolism
- •Dysfunctional adrenergic control
- •Abnormal immunologic processes
- •Oxidative damage
- •Other toxic influences
- •OPTIC NERVE CUPPING AND ATROPHY
- •CLINICAL FEATURES
- •FINDINGS
- •DIFFERENTIAL DIAGNOSIS
- •TREATMENT
- •INDICATIONS
- •GOALS
- •Target pressure
- •TYPES OF TREATMENT
- •PROGNOSIS
- •THE GLAUCOMA SUSPECT AND OCULAR HYPERTENSION
- •EPIDEMIOLOGY OF OCULAR HYPERTENSION
- •RISK FACTORS FOR DEVELOPMENT OF OPEN-ANGLE GLAUCOMA
- •TREATMENT
- •NORMAL-TENSION GLAUCOMA
- •PATHOGENESIS
- •CLINICAL FEATURES
- •DIFFERENTIAL DIAGNOSIS
- •WORK-UP
- •TREATMENT
- •REFERENCES
- •Secondary open angle glaucoma
- •PIGMENTARY GLAUCOMA
- •EXFOLIATION SYNDROME (PSEUDOEXFOLIATION SYNDROME)
- •CORTICOSTEROID GLAUCOMA
- •LENS-INDUCED GLAUCOMA
- •PHACOLYTIC GLAUCOMA
- •LENS-PARTICLE GLAUCOMA
- •PHACOANAPHYLAXIS
- •GLAUCOMA AFTER CATARACT SURGERY
- •GLAUCOMA FROM VISCOELASTIC SUBSTANCES
- •GLAUCOMA WITH PIGMENT DISPERSION FROM INTRAOCULAR LENSES
- •UVEITIS-GLAUCOMA-HYPHEMA SYNDROME
- •GLAUCOMA FROM VITREOUS IN THE ANTERIOR CHAMBER
- •GLAUCOMA AFTER TRAUMA
- •CHEMICAL BURNS
- •ELECTRIC SHOCK
- •RADIATION
- •PENETRATING INJURIES
- •CONTUSION INJURIES
- •GLAUCOMA ASSOCIATED WITH INTRAOCULAR HEMORRHAGE
- •GHOST-CELL GLAUCOMA
- •HEMOLYTIC GLAUCOMA
- •HEMOSIDEROSIS
- •HYPHEMA
- •RETINAL DETACHMENT AND GLAUCOMA
- •SCHWARTZ SYNDROME
- •GLAUCOMA AFTER VITRECTOMY
- •GLAUCOMA WITH UVEITIS
- •FUCHS’ HETEROCHROMIC IRIDOCYCLITIS
- •GLAUCOMATOCYCLITIC CRISIS
- •HERPES SIMPLEX
- •HERPES ZOSTER
- •SARCOIDOSIS
- •JUVENILE RHEUMATOID ARTHRITIS
- •SYPHILIS
- •INTRAOCULAR TUMORS AND GLAUCOMA
- •AMYLOIDOSIS
- •ELEVATED EPISCLERAL VENOUS PRESSURE
- •SUPERIOR VENA CAVA OBSTRUCTIONS
- •THYROID EYE DISEASE
- •ARTERIOVENOUS FISTULAS
- •STURGE-WEBER SYNDROME
- •IDIOPATHIC ELEVATIONS
- •REFERENCES
- •TERMINOLOGY
- •CLASSIFICATION
- •SYNDROME CLASSIFICATION
- •PRIMARY GLAUCOMA
- •CLINICAL ANATOMIC CLASSIFICATION
- •Isolated trabeculodysgenesis
- •Iridodysgenesis
- •Anterior stromal defects
- •Structural iris defects
- •Corneodysgenesis
- •CLINICAL PRESENTATION
- •EXAMINATION
- •Office examination
- •Examination under anesthesia
- •Intraocular pressure measurement
- •Corneal measurements: diameter and central thickness
- •Axial length measurement
- •Gonioscopy
- •Ophthalmoscopy
- •Cycloplegic refraction
- •Systemic evaluation
- •PRIMARY CONGENITAL GLAUCOMA
- •INCIDENCE
- •GENETICS AND HEREDITY
- •PATHOPHYSIOLOGY
- •DIFFERENTIAL DIAGNOSIS
- •Other glaucomas
- •Other causes of corneal enlargement or clouding
- •Other causes of epiphora or photophobia
- •Other optic nerve abnormalities
- •MANAGEMENT
- •Preoperative management
- •Initial surgery
- •Follow-up evaluations
- •Filtering surgery
- •Synthetic drainage devices
- •Cyclodestructive procedures
- •Long-term follow-up, management, and prognosis
- •Late developing primary congenital glaucoma
- •GLAUCOMA ASSOCIATED WITH OTHER CONGENITAL ANOMALIES
- •FAMILIAL HYPOPLASIA OF THE IRIS WITH GLAUCOMA
- •DEVELOPMENTAL GLAUCOMA WITH ANOMALOUS SUPERFICIAL IRIS VESSELS
- •ANIRIDIA
- •STURGE-WEBER SYNDROME (ENCEPHALOFACIAL ANGIOMATOSIS, ENCEPHALOTRIGEMINAL ANGIOMATOSIS)
- •NEUROFIBROMATOSIS (VON RECKLINGHAUSEN’S DISEASE)
- •PIERRE ROBIN AND STICKLER SYNDROMES
- •SKELETAL DYSPLASTIC SYNDROMES
- •CORNEODYSGENESIS
- •Axenfeld’s anomaly
- •Rieger’s anomaly and syndrome
- •PETER’S ANOMALY
- •LOWE SYNDROME (OCULOCEREBRORENAL SYNDROME)
- •MICROCORNEA SYNDROMES
- •RUBELLA
- •CHROMOSOME ABNORMALITIES
- •BROAD THUMB SYNDROME (RUBENSTEIN–TAYBI SYNDROME)
- •SECONDARY GLAUCOMA IN INFANTS
- •PERSISTENT FETAL VASCULATURE (PERSISTENT HYPERPLASITIC PRIMARY VITREOUS)
- •RETINOPATHY OF PREMATURITY (RETROLENTAL FIBROPLASIAS)
- •LENS-RELATED GLAUCOMAS
- •Aphakic pediatric glaucoma
- •Subluxation and pupillary block
- •Marfan syndrome
- •Homocystinuria
- •Spherophakia and pupillary block
- •Weill-Marchesani and GEMSS syndromes
- •TUMORS
- •Retinoblastoma
- •Juvenile xanthogranuloma
- •INFLAMMATION
- •Juvenile rheumatoid arthritis
- •STEROID GLAUCOMA IN CHILDREN
- •NEOVASCULAR GLAUCOMA
- •TRAUMA
- •REFERENCES
- •Genetics of glaucoma
- •BASIC GENETICS
- •GENETIC NOMENCLATURE
- •PRIMARY OPEN-ANGLE, NORMAL-TENSION, AND JUVENILE-ONSET OPEN-ANGLE GLAUCOMA
- •TIGR/MYOCILIN
- •OPTINEURIN
- •OTHER GENES IN OPEN-ANGLE GLAUCOMA
- •EXFOLIATION SYNDROME AND GLAUCOMA
- •GLAUCOMA ASSOCIATED WITH DEVELOPMENTAL DISORDERS
- •PRIMARY CONGENITAL GLAUCOMA
- •AXENFELD-RIEGER ANOMALY
- •ANIRIDIA
- •NAIL PATELLA SYNDROME
- •RENAL TUBULAR ACIDOSIS
- •SUMMARY
- •REFERENCES
- •DIAGNOSIS
- •IDENTIFYING GLAUCOMA SUSPECTS
- •DETERMINING ADEQUACY OF TREATMENT
- •TREATMENT FOLLOW-UP
- •DOCUMENTATION OF PROGRESS
- •PATIENT EDUCATION
- •EFFECTIVE JUDGMENT
- •REFERENCES
- •TARGET PRESSURE
- •MEDICAL THERAPY
- •ADVANTAGES
- •DISADVANTAGES
- •SURGICAL THERAPY
- •ADVANTAGES
- •DISADVANTAGES
- •BASIC PHARMACOLOGY
- •BIOAVAILABILITY OF TOPICAL OCULAR MEDICATION
- •TEAR FILM
- •CORNEAL BARRIERS
- •DRUG FORMULATION
- •DRUG ELIMINATION
- •COMPLIANCE
- •GENERAL SUGGESTIONS FOR MEDICAL TREATMENT OF GLAUCOMA
- •ESTABLISH A TARGET PRESSURE
- •ADJUST THE TREATMENT PROGRAM TO THE PATIENT AND HIS OR HER LIFESTYLE
- •WHEN THERAPY IS INEFFECTIVE, SUBSTITUTE RATHER THAN ADD DRUGS
- •CONTINUALLY MONITOR THE TARGET PRESSURE
- •ASK ABOUT AND MONITOR OCULAR AND SYSTEMIC SIDE EFFECTS
- •SIMPLIFY AND REDUCE TREATMENT WHEN POSSIBLE
- •TEACH PATIENTS THE PROPER TECHNIQUE FOR INSTILLING EYEDROPS
- •PROVIDE WRITTEN INSTRUCTIONS
- •COMMUNICATE WITH THE PATIENT’S FAMILY PHYSICIAN
- •ASK ABOUT PROBLEMS WITH THE MEDICAL REGIMEN
- •CONSIDER DEFAULTING AS AN EXPLANATION FOR THE FAILURE OF MEDICAL TREATMENT
- •EDUCATE PATIENTS ABOUT THEIR ILLNESS AND ITS TREATMENT
- •STOP TREATMENT PERIODICALLY TO DETERMINE CONTINUING EFFECTIVENESS
- •MEASURE INTRAOCULAR PRESSURE AT DIFFERENT TIMES OF THE DAY AND AT DIFFERENT INTERVALS AFTER THE LAST ADMINISTRATION OF MEDICATION
- •RECOMMEND COMPARISON SHOPPING FOR MEDICATIONS
- •SUMMARY
- •REFERENCES
- •Prostaglandins
- •MECHANISM OF ACTION
- •DRUGS IN CLINICAL USE
- •LATANOPROST (XALATAN, PHXA41)
- •BIMATOPROST
- •TRAVOPROST
- •FIXED COMBINATION AGENTS
- •SIDE EFFECTS
- •SUGGESTIONS FOR USE
- •REFERENCES
- •MECHANISM(S) OF ACTION
- •EPINEPHRINE
- •DIPIVEFRIN
- •NOREPINEPHRINE
- •Phenylephrine
- •Clonidine
- •Apraclonidine
- •Brimonidine
- •Isoproterenol
- •Salbutamol
- •Others
- •DOPAMINERGIC AGONISTS
- •ADRENERGIC POTENTIATORS
- •MONOAMINE OXIDASE AND CATECHOL O-METHYLTRANSFERASE INHIBITORS
- •6-HYDROXYDOPAMINE
- •PROTRIPTYLINE
- •GUANETHIDINE (ISMELIN)
- •NONADRENERGIC ACTIVATORS OF ADENYLATE CYCLASE
- •DRUGS IN CLINICAL USE
- •Epinephrine (Eppy, Epinal, Epifrin, and generics)
- •Dipivefrin (Propine and generics)
- •Suggestions for use
- •Side effects
- •Clonidine
- •Prophylaxis in anterior segment laser surgery
- •Argon laser trabeculoplasty
- •Laser iridotomy
- •Nd:YAG laser posterior capsulotomy
- •Management of acute pressure rises
- •Management of open-angle and other chronic glaucomas
- •Combination therapy
- •Side effects
- •Suggestions for use
- •SUMMARY
- •REFERENCES
- •Adrenergic antagonists
- •MECHANISM OF ACTION
- •DRUGS IN CLINICAL USE
- •TIMOLOL MALEATE
- •TIMOLOL HEMIHYDRATE
- •BETAXOLOL
- •LEVOBUNOLOL
- •CARTEOLOL
- •METIPRANOLOL
- •PROPRANOLOL
- •ATENOLOL
- •PINDOLOL
- •NADOLOL
- •METAPROLOL
- •LABETOLOL
- •SUGGESTIONS FOR USE
- •OPEN-ANGLE GLAUCOMA
- •ANGLE-CLOSURE GLAUCOMA
- •SECONDARY GLAUCOMA
- •GLAUCOMA IN CHILDREN
- •BLOOD FLOW AND NEUROPROTECTION
- •SIDE EFFECTS
- •OCULAR
- •SYSTEMIC
- •OTHER ADRENERGIC ANTAGONISTS
- •Thymoxamine
- •Dapiprazole
- •Bunazosin
- •Prazosin
- •Others
- •REFERENCES
- •Carbonic anhydrase inhibitors
- •MECHANISM OF ACTION
- •DIRECT EFFECT ON AQUEOUS HUMOR FORMATION
- •INDIRECT EFFECT ON AQUEOUS HUMOR FORMATION
- •DRUGS IN CLINICAL USE
- •TOPICAL CARBONIC ANHYDRASE INHIBITORS
- •Dorzolamide
- •Brinzolamide
- •SYSTEMIC CARBONIC ANHYDRASE INHIBITORS
- •Acetazolamide
- •Methazolamide
- •Ethoxzolamide
- •Dichlorphenamide
- •SIDE EFFECTS
- •TOPICAL CARBONIC ANHYDRASE INHIBITORS
- •ORAL CARBONIC ANHYDRASE INHIBITORS
- •CONTRAINDICATIONS
- •Acidosis and sickling of red blood cells
- •Other severe symptoms
- •Retinal-choroidal blood flow and neuroprotection
- •SUGGESTIONS FOR USE
- •ANGLE-CLOSURE GLAUCOMA
- •OPEN-ANGLE GLAUCOMA
- •SECONDARY GLAUCOMA
- •INFANTILE AND JUVENILE GLAUCOMA
- •OTHER USES
- •REFERENCES
- •Cholinergic drugs
- •MECHANISMS OF ACTION
- •ANGLE-CLOSURE GLAUCOMA
- •OPEN-ANGLE GLAUCOMA
- •DRUGS IN CLINICAL USE
- •DIRECT-ACTING CHOLINERGIC AGENTS
- •Acetylcholine
- •Pilocarpine
- •Alternative drug delivery systems
- •Methacholine (Mecholyl)
- •Carbachol
- •Aceclidine (Glaucostat)
- •INDIRECT (ANTICHOLINESTERASE) AGENTS
- •Echothiophate iodide (phospholine iodide)
- •Demecarium bromide (Humorsol, Tosmilen)
- •Isoflurophate (Floropryl, di-isopropyl fluorophosphate, Dyflos)
- •Physostigmine (eserine)
- •Neostigmine (prostigmine)
- •SIDE EFFECTS
- •OCULAR
- •SYSTEMIC
- •SUGGESTIONS FOR USE
- •EXAMINATION
- •CONTRAINDICATIONS
- •REFERENCES
- •Hyperosmotic agents
- •MECHANISMS OF ACTION
- •DRUGS IN CLINICAL USE
- •ORAL AGENTS
- •Glycerol
- •Isosorbide
- •Ethyl alcohol
- •INTRAVENOUS AGENTS
- •Mannitol
- •Urea
- •SIDE EFFECTS
- •SUGGESTIONS FOR CLINICAL USE
- •ANGLE-CLOSURE GLAUCOMA
- •SECONDARY GLAUCOMA
- •CILIARY BLOCK (MALIGNANT) GLAUCOMA
- •TOPICAL HYPEROSMOTIC AGENTS
- •OTHER
- •REFERENCES
- •General aspects of laser therapy
- •GENERAL ASPECTS OF LASER THERAPY
- •TISSUE EFFECTS OF LASER
- •THERMAL EFFECTS (PHOTOCOAGULATION, PHOTOVAPORIZATION)
- •PHOTODISRUPTION
- •PHOTOABLATION
- •PHOTOCHEMICAL EFFECTS
- •GENERAL PREPARATION OF THE PATIENT
- •BASIC LASER SAFETY
- •REFERENCES
- •LASER PERIPHERAL IRIDOTOMY
- •INDICATIONS
- •TYPES OF LASER
- •GENERAL PREPARATION
- •ND:YAG LASER IRIDOTOMY
- •ARGON OR SOLID-STATE LASER IRIDOTOMY
- •LIGHT BROWN IRIS
- •Dark brown iris
- •Light blue iris
- •COMPLICATIONS OF LASER IRIDOTOMY
- •Iritis
- •Pressure elevation
- •Cataract
- •Hyphema
- •Corneal epithelial injury
- •Endothelial damage
- •Corneal stroma
- •Failure to perforate
- •Late closure
- •Retinal burn
- •Aphakia and pseudophakia with pupillary block
- •LASER IRIDOPLASTY (GONIOPLASTY)
- •PLATEAU IRIS
- •NANOPHTHALMOS
- •LASERS IN MALIGNANT GLAUCOMA
- •REFERENCES
- •LASER TRABECULOPLASTY
- •HISTORY
- •RESULTS
- •SELECTIVE LASER TRABECULOPLASTY
- •Concept
- •Mechanism
- •Technique
- •Patient preparation
- •Procedure
- •POSTOPERATIVE TREATMENT
- •OUTCOMES
- •CONTRAINDICATIONS
- •AS INITIAL THERAPY
- •PREDICTORS OF OUTCOME
- •APHAKIC AND PSEUDOPHAKIC OPEN-ANGLE GLAUCOMA
- •COMPLICATIONS
- •Intraocular pressure elevation
- •Sustained intraocular pressure increase
- •Hyphema
- •Peripheral anterior synechiae
- •Iritis
- •Uveitis
- •EXCIMER LASER TRABECULOSTOMY
- •Concept
- •Technique
- •Outcomes
- •OTHER LASER SCLEROSTOMY TECHNIQUES
- •REFERENCES
- •CYCLOPHOTOCOAGULATION
- •OTHER LASER PROCEDURES
- •SEVERING OF SUTURES
- •REOPENING FAILED FILTRATION SITES
- •CYCLODIALYSIS AND LASER
- •LASER SYNECHIALYSIS
- •GONIOPHOTOCOAGULATION
- •PHOTOMYDRIASIS (PUPILLOPLASTY)
- •REFERENCES
- •General surgical care
- •THE SURGICAL DECISION
- •PREOPERATIVE CARE
- •INSTRUCTIONS TO THE PATIENT
- •OUTPATIENT VERSUS INPATIENT SURGERY
- •PREOPERATIVE MEDICATIONS
- •OPERATIVE CARE
- •THE OPERATING ROOM
- •ANESTHESIA
- •EQUIPMENT
- •POSTOPERATIVE CARE
- •ACTIVITY
- •MEDICATIONS
- •REFERENCES
- •Glaucoma outflow procedures
- •GENERAL CONSIDERATIONS
- •EXTERNAL FILTRATION SURGERY
- •GUARDED PROCEDURES
- •FULL-THICKNESS PROCEDURES
- •RESULTS OF EXTERNAL FILTRATION SURGERY
- •THE CONJUNCTIVAL FLAP
- •LIMBUS-BASED FLAP
- •FORNIX-BASED FLAP
- •EXCISION OF TENON’S CAPSULE
- •GUARDED FILTRATION PROCEDURE
- •TRABECULECTOMY
- •Indications
- •Standard technique
- •Moorfields Safer Surgery System technique
- •Results
- •Surgical options and modifications
- •Triangular versus rectangular flap
- •Postoperative lasering, adjustment, or release of sutures
- •Wound-healing retardants
- •FULL-THICKNESS FILTRATION PROCEDURES
- •THERMAL SCLEROSTOMY (SCHEIE PROCEDURE)
- •SCLERECTOMY
- •Posterior lip sclerectomy
- •Anterior lip sclerectomy
- •TREPHINATION
- •IRIDENCLEISIS
- •GLAUCOMA DRAINAGE DEVICES
- •THE MOLTENO IMPLANT
- •Techniques
- •SCHOCKET PROCEDURE
- •KRUPIN VALVE AND EX-PRESS IMPLANT
- •AHMED VALVE
- •BAERVELDT IMPLANT
- •RESULTS AND COMPLICATIONS OF DRAINAGE DEVICES
- •REFERENCES
- •CATARACT SURGERY IN THE GLAUCOMATOUS EYE
- •TYPES OF GLAUCOMA AND THEIR INFLUENCE ON CATARACT MANAGEMENT
- •SELECTING THE APPROPRIATE SURGICAL APPROACH
- •SELECTING THE APPROPRIATE PROCEDURE: HISTORICAL CONSIDERATIONS
- •SURGICAL TECHNIQUES FOR COMBINED PROCEDURES
- •GENERAL PREOPERATIVE CONSIDERATIONS
- •SMALL-INCISION COMBINED SURGERY
- •Incision sites
- •Fornix versus limbal conjunctival flap
- •Scleral flap
- •Antimetabolite use
- •Managing the small pupil
- •Phacoemulsification techniques
- •Intraocular lens selection
- •Trabeculectomy formation
- •Flap closure
- •Postoperative medical management
- •EXTRACAPSULAR CATARACT EXTRACTION COMBINED SURGERY
- •Miotic pupil
- •Incision construction
- •CATARACT SURGERY WITH PRE-EXISTING FILTRATION BLEB
- •REFERENCES
- •BUTTONHOLING THE CONJUNCTIVA
- •THE SHALLOW AND FLAT ANTERIOR CHAMBER
- •FLAT ANTERIOR CHAMBER WITH HYPOTONY
- •FLAT ANTERIOR CHAMBER IN NORMOTENSIVE AND HYPERTENSIVE EYES
- •CILIARY BLOCK (MALIGNANT GLAUCOMA)
- •SUPRACHOROIDAL HEMORRHAGE (SCH)
- •INTRAOPERATIVE FLAT ANTERIOR CHAMBER
- •HYPHEMA
- •LARGE HYPHEMA
- •INTRAOCULAR INFECTION
- •SYMPATHETIC OPHTHALMIA
- •FILTRATION FAILURE
- •DIGITAL PRESSURE
- •FAILURE DURING THE FIRST POSTOPERATIVE WEEK
- •PLUGGED SCLEROSTOMY SITE
- •RETAINED VISCOELASTIC MATERIAL
- •TIGHT SCLERAL FLAP: RELEASABLE SUTURES AND LASER SUTURE LYSIS
- •INADEQUATE OPENING OF DESCEMET’S MEMBRANE
- •ENCAPSULATED BLEB
- •REOPERATION AFTER FAILED FILTRATION
- •REVISION OF ENCYSTED BLEB
- •Needling of failed blebs
- •Slit-lamp or minor surgery setting
- •Operating room setting
- •FAILED FILTRATION WITH NO BLEB
- •BLEB COMPLICATIONS AND MANAGEMENT
- •THIN-WALLED BLEBS
- •DIFFUSE BLEBS
- •OVERFUNCTIONING BLEBS
- •DELLEN
- •HYPOTONOUS MACULOPATHY
- •LATE HYPOTONY AFTER FILTERING SURGERY
- •HYPOTONY WITH OCCULT FILTERING ‘BLEB’
- •HYPOTONY WITH OCCULT CYCLODIALYSIS CLEFTS
- •HYPOTONY WITH AQUEOUS SUPPRESSION THERAPY IN CONTRALATERAL EYE
- •HYPOTONY FROM RETINAL DETACHMENT
- •HYPOTONY FROM IRITIS OR ISCHEMIA
- •REFERENCES
- •SURGERY FOR INFANTILE AND JUVENILE GLAUCOMA
- •GONIOTOMY
- •Preoperative considerations
- •Intraoperative procedures
- •Complications
- •Practice goniotomy
- •Other ab-interno angle surgery
- •TRABECULOTOMY AB EXTERNO
- •EVALUATION OF GONIOTOMY AND TRABECULOTOMY
- •COMBINED TRABECULOTOMY AND TRABECULECTOMY
- •TRABECULODIALYSIS
- •MISCELLANEOUS PROCEDURES
- •Goniosynechialysis
- •Cyclocryotherapy
- •Retrobulbar alcohol injection
- •Earlier procedures
- •REFERENCES
- •New ideas in glaucoma surgery
- •INTRODUCTION
- •NON-PENETRATING GLAUCOMA SURGERY
- •VISCOCANALOSTOMY
- •BYPASS INTRASCLERAL CHANNELS (NON-PENETRATING DEEP SCLERECTOMY)
- •SHUNTS INTO SCHLEMM’S CANAL
- •TRABECTOME®
- •SHUNTS INTO THE SUPRACHOROIDAL SPACE
- •SUMMARY
- •REFERENCES
- •Challenges for the new century
- •PATHOPHYSIOLOGY
- •CLASSIFICATION AND DIAGNOSIS
- •SCREENING
- •TREATMENT
- •CONCLUSION
- •REFERENCES
- •Appendix
- •GLAUCOMA CONSENSUS
- •GLAUCOMA DIAGNOSIS – STRUCTURE AND FUNCTION (2004)
- •CONSENSUS STATEMENTS
- •Structure
- •Function
- •Function and structure
- •GLAUCOMA SURGERY – OPEN ANGLE GLAUCOMA (2005)
- •CONSENSUS STATEMENTS
- •Indications for glaucoma surgery
- •Argon laser trabeculoplasty
- •Wound healing
- •Trabeculectomy
- •Combined cataract/trabeculectomy
- •Aqueous shunting procedures with glaucoma drainage devices
- •Comparison of procedures: trabeculectomy versus aqueous shunting procedures with glaucoma drainage devices
- •Non-penetrating glaucoma drainage surgery
- •Comparison of trabeculectomy with non-penetrating drainage glaucoma surgery in open-angle glaucoma
- •Cyclodestruction
- •Comparison of cyclophotocoagulation and glaucoma drainage device implantation
- •ANGLE CLOSURE AND ANGLE-CLOSURE GLAUCOMA (2006)
- •CONSENSUS STATEMENTS
- •Management of acute angle closure crisis
- •Surgical management of primary angle-closure glaucoma
- •Laser and medical treatment of primary angle-closure glaucoma
- •Laser and medical treatment of primary angle-closure glaucoma
- •Detection of primary angle closure and angle-closure glaucoma
- •INTRAOCULAR PRESSURE (2007)
- •CONSENSUS STATEMENTS
- •Measurement of intraocular pressure
- •Intraocular pressure as a risk factor for glaucoma development & progression
- •Epidemiology of intraocular pressure
- •Clinical trials and intraocular pressure
- •Target intraocular pressure in clinical practice
- •Index
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Visual field theory and methods |
8 |
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Fig. 8-7 Patient viewing ‘snowfield’ on computer monitor. Defects are noticed by the patient as smudges or fuzzy areas on screen.
patient must undergo a full visual field examination to establish a baseline against which future change can be measured. Therefore, in persons suspected of having visual field defects, screening programs and other fast strategies that reduce examination time at the expense of evaluating the critical sensitivity area within 5 dB of threshold are of questionable value.23 Screening tests are used most appropriately to diagnose pathology rather than to follow or quantitate the degree of damage in a patient known or suspected of having disease.
Other Static Testing Techniques
Single-stimulus level static testing was used commonly in some of the early computerized perimeters. Because the visual threshold slopes from the center to the periphery of vision, a single-stimu- lus intensity cannot be effective in testing a large area of the retina. This technique is useful only as a relatively crude screening method. A variety of innovative screening techniques has been developed to aid clinicians in obtaining the maximum amount of useful information in the minimum amount of time. A few of these bear mention for illustrative purposes.
Noisefield perimetry, also known as white-noise perimetry or
campimetry, is performed by having the patient observe a computer screen (Fig. 8-7) or home television set.28–30 The screen projects
a ‘noise’ pattern of small (roughly 1–4 mm), irregularly shaped dark and bright spots oscillating at 50 Hz. Patients with localized defects notice the defective region as a smudge or blank area on the screen. In simple terms, they detect the noise pattern in normal regions of the field, and its absence in the abnormal areas is perceivable. Detection takes only seconds in alert patients, but not all patients can cooperate fully with the test requirements. The information gained is useful mainly for screening.31–33 Optokinetic perimetry is a novel approach to visual field screening in which the patient is presented a series of cards with static stimuli arranged in a set pattern. While
maintaining steady fixation, the patient is asked how many spots she sees.34–36 Stimuli in defective areas of the field are not detected, and
by evaluating the points missed during the test, the examiner can gain a fairly clear idea of the nature and extent of the field loss.37–40
This method is very fast, taking perhaps only 30–50% of the total time needed for screening fields conventionally. These methods are used rarely, if at all, in clinical practice.
The Swedish Interactive Test Algorithm (SITA) was developed to address the issue of patient fatigue and discomfort during tedious full-threshold static automated perimetry examinations, which can require 30 minutes or more per eye. Long, boring examinations are stressful for patients; fatigue and a resultant lack of concentration can decrease test reliability. The SITA was developed to reduce testing time without reducing reliability or sensitivity. The basic approach is fairly straightforward, although the programming required to achieve these aims was very sophisticated. The SITA relies on a continually updated model of the patient’s predicted field, based on all of the information available on the patient, including, importantly, answers to test questions as the test itself progresses.17 The program is termed ‘interactive’ because it changes the questions it asks based on the patient’s responses, in real time. In addition to predicting the model of the patient’s field, the program assesses the certainty of its prediction at each test point. Testing is interrupted as soon as a predetermined level of certainty is reached. This is in contrast to standard testing algorithms in which testing follows a more rigid pattern, whether or not additional information will further refine the model.
The initial model of the patient’s field is based on a large databank of normal and glaucomatous fields, adjusted for age. As test points within the field undergo threshold evaluation, the model is updated. If, for example, the first few test points are characteristic of a generally depressed field, subsequent stimuli will be brighter than if the initial test points had suggested a normal field. An important feature of SITA is that it uses all of the available information as it refines its model.As more information is accumulated, the program develops a more accurate prediction of the final field, and can confirm its prediction with fewer additional test questions. During an initial evaluation, SITA used fewer test points in normal and glaucomatous fields. Because the interval between stimulus presentations is also adjusted, the actual testing time can be reduced by an even greater amount. In clinical tests, SITA standard examinations require less than half the time required to perform a full-threshold exam.41 Because of its combination of speed, accuracy, and patient acceptance, most centers and offices with SITA equipped perimeters use this as their basic testing strategy.
The future of visual field testing
The current generation of computerized perimeters allows placement of stimuli of varying sizes, intensities, and colors into backgrounds of varying intensities, and they accurately chart the patient’s responses.42 This flexibility facilitates design of an almost infinite number of testing protocols. Recent improvements have involved both hardware and software. A wide variety of test and interpretation protocols are in use, and more are being developed continually. Most commercially available protocols have been standardized against groups of normal patients. A few disease-specific protocols
have been standardized against groups of patients with the target condition.4,43–47 Although these programs do not fully replace care-
ful interpretation by a trained observer, they certainly help to guide us toward more consistent evaluation of visual field information.
Differential light sensitivity is a rather primitive retinal function. Quigley and Green found that up to 50% of retinal nerve fibers may be lost before a diagnostic glaucomatous visual field defect is detected by manual kinetic measurement.48 Computerized static perimetry with statistical analysis of the results is more sensitive,49
95
part
3 clinical examination of the eye
but some amount of nerve fiber loss precedes even computerized field loss in most cases.50 These lost nerve fibers assist in other visual functions that may be more sophisticated than simple differential light sensitivity. One of the more intriguing ways that this has been investigated is with blue-on-yellow, or short wavelength, automated perimetry (SWAP). A series of studies has indicated that the short wavelength-sensitive (blue) system may be more sensitive to early glaucoma.51–53 The test is similar to conventional perimetry except blue stimuli are projected on a yellow background to isolate the short wavelength-sensitive system. The results of these studies have been quite interesting. In one study, Johnson and co-workers54 tested 38 ocular hypertensive patients and 62 normal controls with conventional white-on-white (w/w) perimetry and subsequently with SWAP. All 38 ocular hypertensive patients had normal w/w perimetry at the time the study began. Nine of these eyes had a defect detected by SWAP at the beginning of the study. Five years later, 5 of the 9 eyes that initially showed a SWAP defect but were normal by w/w perimetry had developed w/w visual field loss. The w/w defects were in the same locations of the visual field as the SWAP defects, but the SWAP defects were larger. No eye that was initially normal on SWAP testing developed w/w field loss during the period of study. Thus SWAP perimetry was very sensitive (100%) for early glaucoma; its specificity (using w/w defects as the standard) was 55% (5/9) at 5 years, but this may rise with longer follow-up.
Other studies have generated similar findings. The general pattern is that SWAP defects, although similar in location and shape, appear earlier and are larger than subsequent w/w defects.55–58 This method is not entirely without cost, however. Short wavelength, automated perimetry takes longer than equivalent w/w perimetry, and increased patient fatigue and decreased dynamic range may contribute to significantly higher fluctuation values. Newer com-
binations of SWAP and more interactive programs that shorten test time will make SWAP testing more acceptable to patients.59,60
The increased testing time and fluctuation have limited the use of SWAP in routine clinical settings. It is employed most frequently to help confirm the diagnosis, or detect subtle progression in a patient with early disease.
In addition to perimetric techniques, there are a host of other psychophysical methods of detecting and following glaucomatous damage. Some of these are discussed in Chapter 11.
Combined static and kinetic perimetry
Combined static and kinetic perimetry uses the speed of kinetic perimetry and the sensitivity of static testing. It is used routinely in manual perimetry, and rarely with automated perimeters. Generally, the peripheral field and scotomata are defined by kinetic methods, and the central field is examined by static perimetry. With manual perimetry, a threshold stimulus is chosen for testing the central field. This stimulus is chosen by a variety of methods, but commonly it is the weakest stimulus visible at the point either 15° above or 15° below the horizontal meridian 25° temporal to fixation.
Aulhorn and Harms,3 Armaly,61–63 Drance and Anderson,24 and Rock and co-workers64 suggested methods using this approach to rapidly detect and define scotomata. The threshold stimulus is used to kinetically define the central field and any scotomata demonstrated by the static presentations. Static stimuli are presented at various locations for no more than 1 second. Hesitant or absent patient response indicates a potential defect, which then can be more completely analyzed by kinetic perimetry using varying stimulus sizes and intensities (Fig. 8-8).
With automated perimetry, the central field is examined in the standard static fashion, and one or two peripheral isopters are
examined to avoid missing defects that do not involve the central field.65–67 The peripheral field can be examined by static-
threshold perimetry,but this is a time-consuming and tedious process. Full-threshold testing of the periphery costs a great deal in terms of patient fatigue and satisfaction for relatively little gain, and is therefore performed rarely. Static twoor three-zone screening tests are a reasonable compromise that allow the examiner to de-emphasize, but not ignore, the periphery.
Fig. 8-8 Goldmann visual field chart illustrating both static (dots) and kinetic (arrows) points of examination. Note that 72 points
are tested statically with a threshold target in the central field. This is considered a reliable search for early glaucomatous field defects.
The I4e target is used to check for nasal step in the peripheral field. Testing of the peripheral temporal field for a step will identify the occasional patient in whom this is the earliest evidence of glaucomatous damage. Tangent screen can be tested in a similar manner within the central 30° by exposing and hiding the stimulus to stimulate static perimetry.
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7. Hudson C,Wild JM, O’Neill EC: Fatigue effects during a single session of automated static threshold perimetry, Invest OphthalmolVis Sci 35:268, 1994.
8. Wild JM, et al: Long-term follow-up of baseline learning and fatigue effects in the automated perimetry of glaucoma and ocular hypertensive patients,Acta Ophthalmol Scand Suppl 69:210, 1991.
9. Araujo ML, Feuer WJ,Anderson DR: Evaluation
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